Journal
NEUROREPORT
Volume 12, Issue 9, Pages 1841-1845Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200107030-00016
Keywords
demyelination; EAE; HO-1; multiple sclerosis; oligodendrocyte; oxidative stress
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Increasing evidence shows that oxidative stress plays an important role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of the human disease, multiple sclerosis (MS). Heme oxygenase-l (HO-I) is a hear shock protein induced by oxidative stress. HO-I metabolizes heme to the antioxidant bilirubin and carbon monoxide, and represents a powerful endogenous defensive mechanism against free radicals in many diseases. However, the role of this important enzyme in EAE remains unknown. In this study, we showed high expression of HO-I in lesions of EAE, and demonstrated that hemin, an inducer of MO-I, inhibited EAE effectively. In contrast, tin mesoporphyrin, an inhibitor of HO-I, markedly exacerbated EAE. Our results suggest that endogenous HO-I plays an important protective role in EAE, and that targeted induction of HO-I overexpression may represent a new therapy for the treatment of multiple sclerosis. NeuroReport 12:1841-1845 (C) 2001 Lippincott Williams & Wilkins.
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